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Insulin-Induced Hypoglycemia Accelerates Gastric Emptying of Solids and Liquids in Long-Standing Type 1 Diabetes

Department of Medicine (A.R., J.E.S., R.C., D.G., M.H., K.L.J.) and Endocrine and Metabolic Unit (R.B.), Royal Adelaide Hospital, University of Adelaide, Adelaide, South Australia 5005, Australia

Address all correspondence and requests for reprints to: Dr. Karen L. Jones, University of Adelaide, Department of Medicine, Royal Adelaide Hospital, Frome Road, Adelaide, South Australia, 5005, Australia. E-mail: karen.jones{at}adelaide.edu.au.

Context: The rate of gastric emptying of carbohydrate is a major determinant of postprandial glycemia. In healthy subjects and patients with uncomplicated type 1 diabetes, there is evidence that gastric emptying may be accelerated by insulin-induced hypoglycemia.

Objective: The objective was to determine the effects of acute hypoglycemia on gastric emptying in long-standing type 1 diabetes and evaluate whether the response to hypoglycemia is influenced by the rate of gastric emptying during euglycemia and/or autonomic dysfunction.

Design: Gastric emptying of a solid/liquid meal (100 g ^99mTc–minced beef and 150 ml ⁶⁷Ga-EDTA-labeled water) was measured by scintigraphy on 2 separate days, during hypoglycemia and euglycemia.

Setting: These studies took place at the Department of Nuclear Medicine, Positron Emission Tomography, and Bone Densitometry at the Royal Adelaide Hospital.

Patients: Twenty type 1 patients (4 female, 16 male; age, 45.9 ± 2.3 yr; duration of known diabetes, 18.0 ± 2.7 yr) were recruited from outpatient clinics and the Diabetes Centre at the Royal Adelaide Hospital.

Intervention: Hypoglycemia (2.6 mmol/liter) was established 15 min before and maintained for 45 min after meal consumption. On one of the days, autonomic nerve function was evaluated using cardiovascular reflex tests.

Main Outcome Measure: The main outcome measure was gastric emptying during hypoglycemia when compared with euglycemia.

Results: Twelve of the 20 subjects had autonomic neuropathy. Gastric emptying of both solid (P < 0.001) and liquid (P < 0.05) was faster during hypoglycemia. The magnitude of this acceleration was greater when the rate of gastric emptying during euglycemia was slower (solid, percentage retention at 100 min, r = –0.52, P < 0.05; liquid, 50% emptying time, r = –0.82, P < 0.0001, but not influenced by autonomic nerve function).

Conclusions: Insulin-induced hypoglycemia accelerates gastric emptying of solids and liquids in long-standing type 1 diabetes, even in those patients with delayed emptying, and is likely to be an important mechanism in the counter-regulation of hypoglycemia.